We contributed to several rodent studies that investigated sources of variability in response to genetics and environmental agents. In a rat study, we compared several behavioral characteristics between male and female rats exposed to one of several estrogenic compounds. In this study, pregnant rats were exposed to bisphenol A (BPA) or estrogen or nothing (controls) during gestation and their pups were exposed to the same compound after birth, through weaning. Male pups exposed to estrogen experienced puberty later than controls while BPA did not delay puberty. Behavioral tests showed a significant difference between control males and females and this difference remained the same in pups treated with BPA. However, the difference between male and female behavior was narrowed in pups treated with estrogen, in that male behavior became more similar to female rat behavior. In a mouse study, we compared normal mice to mice lacking one of the estrogen receptors. The mice lacking the estrogen receptor tend to be less fertile than normal mice, but the mechanism for the reduced fertility is not known. We found that among the organs involved in fertility, only the ovaries were affected by absence of the receptor and that they did not produce adequate levels of hormones to stimulate ovulation. The chemical, perfluorooctanoic acid (PFOA), is used primarily as an industrial surfactant. It is known to cause liver cancer in rodents, but the mechanism is unclear. Because there is some indication that PFOA activates peroxisome proliferator receptors (PPAR), we studied rats that do not have this receptor (PPAR-alpha knockouts (KO)), along with wild type rats and mice. The PPAR-alpha KO rats demonstrated the same liver lesions in response to PFOA treatment as the wild type rats and mice, indicating that PFOAs mechanism of liver damage is not completely through the PPAR-alpha receptor. Furthermore, electron microscopy of the mouse livers showed extensive changes in the shapes and numbers of mitochondria of the cells, suggesting that peroxisome proliferation is not the mechanism for liver toxicity of PFOA.